Arterial Compression of the Ventro-Lateral Medulla

描述（由申请人提供） 主要研究者（PI）是全职学术神经外科医生， 擅长后颅窝神经血管压迫手术 综合征这项研究事业奖将使他有时间获得 在神经源性疾病中进行进一步以患者为导向的研究所需的技能 并取得临床研究理学硕士学位。 他将在研究和培训期间获得的经验， K23奖将使他成为一名独立的临床研究者， 专注于神经源性高血压的机制，并能够设计和 进行治疗研究。PI有他的承诺和支持 赞助商，部门和机构允许的时间和分配 实现他的研究职业目标所需的资源，并完成他的建议 research.将通过机构K30奖促进培训， a国家卫生研究所支持的全球儿童权利中心。有待检验的假设是， 介导的高血压是由动脉压迫沿着 延髓腹外侧橄榄后沟。 因此，该项目的目标是：1）在人类中建立电 沿延髓腹外侧正常表面的沿着位置， 对刺激敏感并产生升压反应; 2）显示出 这些“压力敏感”区域的动脉压迫 沿着骨髓表面（在目标1中建立）和 交感神经张力和心血管功能 神经性高血压血液动力学和交感神经反应模式 将记录髓表面的电刺激以映射 加压调节神经元组的表面下的位置， 接受后颅窝手术的患者的腹外侧延髓。 关于反应模式的信息将用于第二项研究， 研究这些升压调节的动脉压迫之间的关系 高血压个体的面积和相似的测量模式。 这项研究的结果应该有助于更好地定义生理学 与腹外侧动脉压迫相关的标准 髓质到神经源性高血压。

DESCRIPTION (provided by applicant) The Principal Investigator (PI) is a full time academic neurosurgeon who specializes in surgery of the posterior fossa for neurovascular compression syndromes. This research career award will afford him the time to acquire the skills needed to perform further patient-oriented research in neurogenic hypertension and obtain a Master of Science degree in Clinical Research. The research and training experience he will obtain during the period of the K23 Award will allow him to become an independent clinical investigator with a focus on mechanisms of neurogenic hypertension, and to be able to design and conduct studies on its therapy. The PI has the commitment and support of his sponsor, department and institution to permit the time and allocate the resources needed to attain his research career goals and complete his proposed research. Training will be facilitated through the institutions K30 Award and a NIH supported GCRC. The hypothesis to be tested is that neurogenically mediated hypertension is caused by arterial compression of areas along the retro-olivary sulcus of the ventro-lateral medulla. Therefore the aims of the project are to: 1) electrically establish in humans the locations along the normal surface of the ventro-lateral medulla that are sensitive to stimulation and produce pressor responses; and 2) show an association between arterial compression of these 'pressor-sensitive' areas along the medullary surface (established in Aim 1) and aberrations in sympathetic tone and cardiovascular functions in volunteering subjects with neurogenic hypertension. Hemodynamic and sympathetic response patterns to electrical stimulation of the medullary surface will be recorded to map the location of the pressor-regulating neuronal groups under the surface of the ventro-lateral medulla in patients undergoing surgery of the posterior fossa. This information on response patterns will then be used in a second study to investigate associations between arterial compression of these pressor-regulating areas and similar measured patterns in hypertensive individuals. Results from this research should help to better define the physiologic criteria to be used to relate arterial compression of the ventro-lateral medulla to neurogenic hypertension.